Download The Question of Questions: What is a Gene? Comments on Rolston

Theoretical Medicine and Bioethics (2006) 27:523–534
DOI 10.1007/s11017-006-9021-x
Ó Springer 2006
LENNY MOSS
THE QUESTION OF QUESTIONS: WHAT IS A GENE?
COMMENTS ON ROLSTON AND GRIFFTHS & STOTZ
ABSTRACT. If the question ‘‘What is a gene?’’ proves to be worth asking it must be
able to elicit an answer which both recognizes and address the reasons why the
concept of the gene ever seemed to be something worth getting excited about in the
first place as well analyzing and evaluating the latest develops in the molecular
biology of DNA. Each of the preceding papers fails to do one of these and sufferrs
the consequences. Where Rolston responds to the apparent failure of molecular
biology to make good on the desideratum of the classical gene by veering off into
fanciful talk about ‘‘cybernetic genes,’’
Griffiths and Stotz lose themselves in the molecular fine print and forget to ask
themselves why ‘‘genes’’ should be of any special interst anyway.
KEY WORDS: Aristotle, telo, final cause, formal cause, epigenesis, preformationism, information, cybernetic genes, Gene-P, Marfan Syndrome, nominal genes,
instrumental genes, Kirshner and Gerhart, West-Eberhard
The answer to a philosophical question can lead to many different
outcomes: fundamental insights into states of affairs, uncovering of
conceptual confusions and fine-tuning of conceptual boundaries, or
the turning-over of stones that had hitherto held their ground.
Sometimes, however, the shortcomings of answers may lead to a
higher (or more ‘‘meta’’) level of reflection on why it may have been
the wrong question to ask in the first place. The idea of the gene has
long, and always, been about grasping something fundamental about
the living organism—which is also to say that it does not merit any
intrinsic interest outside the context of what it reveals about the living
organism. Other than perhaps as a historical reflection, from within a
discipline, on the rise and fall of its distinctive concepts, the interest in
the concept of the gene is accountable and subordinate to what if any
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value it has for biology. I will argue that the papers by Rolston and
by Griffiths & Stotz are revealing most of all in this latter sense.
Inasmuch as neither succeeds in offering an account of the concept of
the gene that is simultaneously both lucid and interesting in relation
to the ‘‘big questions’’ of biology, we are provoked to wonder
whether the problem may pertain to the question being asked itself.
The apparent enigma of the gene can only adequately be appreciated from a very wide angle. The point of departure for systematic
and explanatory accounts of the living world, i.e., biology (albeit
before it was called such) was the work of Aristotle. Explicitly
Aristotelian biological enterprises, such as that of Georges Cuvier,
continued well into the 19th century. Even if some combination of
Darwin and Mendel, or perhaps Darwin, Mendel, and Watson &
Crick, have finally rendered any vestiges of Aristotle’s approach
incorrect (as many champions of 20th century biology have held), or
even just redundant, it would still be useful to know just what it is
that we can now answer 2,000 years later that Aristotle could not.
What are the central problems that have occupied these millennia of
biological inquiry to which the solutions of genetic Darwinism must
be held accountable?
For present purposes, I want to pick out from Aristotle two
important insights he got right. Aristotle recognized that living
beings, organisms, must be understood in all respects as ends-untothemselves. What they do, how they are, how they develop and
change can only be understood as being neither random and accidental, nor for the sake of some other good, but only with respect to
the realization of their own good (or telos)—that is, in terms of their
very existence as their own ultimate end. Aristotle’s sense of final
cause captures what microbiology and cell biology have more
recently come to recognize about even single cells: that even microscopic cells can be trained to sustain fluctuations in heat, ionic concentration, toxic exposure, and other such challenges, i.e., that even
single cells exist and act as ends-unto-themselves in ways that we have
yet to exhaustively catalog and explain. The other point that Aristotle
got right was that biology could not be explained reductively on the
basis of the properties of elemental matter as his time understood
these to be. Aristotle’s solution was not to appeal to a transcendent
cause but rather to be a kind of holist about nature. Nature was
understood to be possessed of local purposes. Whereas the final cause
of an artifact, such as a table, is given to it by the artisan (and by
those who use it as a table), the final cause of an organism is present
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within itself and it is inseparable from its formal cause (its phenotypic
form). Organisms, as it were, give themselves their form for the sake
of their own ultimate good as the kinds of beings they are. Final and
formal causes thus impose themselves upon matter, i.e., upon material cause. Matter takes the shape it does, and changes as it does, for
the sake of attaining the final good of being a certain kind of
organism.
The problem with Aristotelian biology begins when we can no
longer ‘‘metaphysically’’ countenance the idea that final cause can exist
within nature (except perhaps for humans). Seventeenth century biologists did not invert the dominance of form and finality over matter.
They simply lifted the latter up into the realm of the transcendent
(creator-god), by way of multiple versions of preformationism.
(Amundson, 2005) The real challenge for a post-seventeenth century,
non-creationist biology has been that of explaining the ‘‘finality of life’’
that Aristotle got right on the basis of some new and enhanced
understanding of material cause. This would be the realization of a
Copernican Revolution in biology.
Much, if not all, of the subsequent history of biology can be seen
as attempts to reconfigure Aristotle’s four causes within the constraints of modern metaphysical assumptions about nature. Preformationism, as set forth by Jan Swammerdam, (Darwin, 1998) for
whom the finality of form was provided at creation, could then
separate the dynamics of the unfolding of form from questions of
finality and thus study formal cause on its own. This led to further
work of nineteenth century morphologists who sought to grasp the
logos of biological form and its transformations. Linnaeus’s taxonomy can also be seen as a work on form pulled apart from finality,
and indeed it was the formal classificatory systematics of the early
18th century that led to the morphological enterprises of the late 18th
and early 19th centuries. (Kant, 1987) Against the objections of his
neo-Aristotelian adversary Buffon, Linnaeus’s taxonomy did not
attempt to reveal the core of an organism’s way of being (its final
cause). It only sought to provide a serviceable method of classification, assuming however that the tableau of the living world, the final
cause of the ordering of living beings, its ‘‘logos’’ was provided from
‘‘above,’’ as it were, by transcendent design. Epigenesists, such as
Buffon and Needham, (Kirchner and Gerhart, 2005) who remained
true to the inseparability of formal with final cause, tried to solve the
problem in a Newtonian spirit at the level of efficient cause. If
Newton could make action at a distance scientifically acceptable,
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then perhaps some form of organizational or formative force could
likewise bring final cause back into the nature of the beast. Such
efforts were of course ultimately ridiculed as ‘‘vitalisms.’’ It was then
Immanuel Kant who both re-articulated a version of the Aristotelian
insight into the irreducibly ‘‘self-purposive’’ character of the living
organism and simultaneously disavowed the possibility of it ever
being explained on the basis of material (and/or efficient)
cause—hence his famous proclamation that there would ‘‘never be a
Newton of a blade of grass.’’ (Moss, 2003)
The widespread conviction (albeit largely tacit) that Kant has been
‘‘disproved’’ and that twentieth century biology has succeeded in
explaining life on a ’material basis’ turns on two central pivots—Darwinism and the idea of the gene. Darwin himself, however,
said no such thing. Darwin offered part of an account of how
adaptive form can result from material conditions, but only in part.
He proposed a theory subject to ‘‘the laws of generation and variation’’—laws that he could neither provide nor purge of any trace of
final cause: so conceived, the evolution of new and adaptive form
could and would come about through ‘‘natural selection.’’
(Nordenskiöld, 1928) Whether the processes of generation and
variation (and thus evolution by natural selection) could be fully
accounted for on a non-teleological material basis was left an open
question. But Darwin was no Darwinian zealot. For Darwin, it was,
in any event, also the case that the ‘‘final cause’’ of the organism did
in fact play a direct role in the subsequent evolution of form since
aesthetic preference (sexual selection) and force of habit were both
understood to be forces of evolutionary change. (Ospovat, 1981)
If one takes it as an unquestioned, albeit often tacit, given that
contemporary biology has succeeded in explaining life in all its forms
and without recourse to any ‘‘illicit’’ notions of immanent final cause,
then one can begin to appreciate the burden that weighs upon the
concept of the gene and to understand a motivating source of some of
the stark peculiarities of Rolston’s article on the concept of the gene.
To begin with, Rolston’s philosophical analysis of the concept of
the gene is not very philosophical at all. Whereas philosophers see
inconsistent claims as provocations that must be analyzed,
challenged, and overcome, journalists see the same as evidence of the
achievement of balance and neutrality—the fair representation of all
sides. Ostensibly, Rolston then writes in the style of the journalist. At
first he steps back and lets the professionals do the talking, but what
the professionals have to say is often inconsistent. Development, we
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are told, has proven to be modular, and so is indeterminate with
respect to any of its modular parts which in themselves may
contribute to alternative phenotypic outcomes. Nonetheless, preformationistic genetics has always assumed that traits are determined by
discrete modular parts (genes), so (somehow) everything is fine. Is
Rolston just so blissfully ignorant of cell and developmental biology
that he does not get the problem or is this a rhetorical sleight of hand
in the service of an as yet to be revealed agenda? After amply
acknowledging the impossibility of even definitively individuating
genes (defining the boundaries of genetic units) at a material level (as
segments in DNA), he turns in a surprising direction that reveals his
larger intentions. What could not be said univocally at the material/
empirical level can suddenly be espoused with certainty at the more
formal-ethereal level of ‘‘information.’’ No longer deferring to the
voices of others, Rolston now proclaims that: ‘‘A gene is a cybernetic
unit, an information fragment. What is conserved is not the matter,
not the organism, not the somatic self, not even the genes, but a
message that can only be conserved if and only if it is distributed,
disseminated. That may be the sine qua non of any complete account
of what a gene is.’’ Having stepped away from the muck of matter,
far-reaching ontological claims can now come fast and furious. While
at the empirical/molecular level we know that a single stretch of
coding DNA on a chromosome may provide the template resource
for potentially hundreds or thousands of downstream RNA and/or
protein products, it is thus problematic at least to refer to a gene as
‘‘representing’’ any one immediate outcome. Having moved to this
more ethereal level, Rolston begins to describe representation in
almost spiritual terms: ‘‘The organism instantiates its genetic types;
survival of the gene type is what counts. Its genes code the kind,
representatively; and the organism, an expression of the kind,
presents and re-presents the kind in the world.’’
Eventually Rolson’s discussion of the ‘‘cybernetic’’ gene is just as
inconsistent and equivocal (or perhaps journalistically ‘‘balanced’’) as
his earlier, ostensibly second-hand account of Mendelian and
molecular genes. Cybernetic genes encode ‘‘how to live on land or
how to nurse a baby,’’ and yet ‘‘the organism selects what to play,
and improvises on the themes, cutting and splicing here and there,
depending on the circumstances and needs of the organism.’’ It is
now the organism that is the reader and the genome that is merely a
stereotyped script, or the organism that is a cook and the genome
merely a recipe. ‘‘Cybernetic genes are open as much as they are
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deterministic,’’ but then again ‘‘Genes carry the information that the
elk should flee the approaching hunter or that the plant should
secrete repair products and rebuild roots prospective to survival
through the winter’’ (even if genetics cannot yet provide a taxonomy
of such information). So why then make the move at all toward the
immateriality of the cybernetic gene and its information and representations, thereby (more than) risking a descent into nonsense and
vapid flights of fancy? The give-away clue can be found in Rolston’s
own hand: ‘‘What genes have is a Ôtelos,Õ an Ôend.Õ Magmas crystallizing into rocks, and rivers flowing downhill have results but no such
Ôend.Õ Organisms are biological agents; the phenotypes are doing
something, maintaining their form of life; and they succeed because
within them are genes which are also biological agents, doing
something, maintaining this form of life. Genes are proactive.’’
Rolston, we can now see, is caught in a contemporary dilemma.
The living organism, as Aristotle observed, is characterized by being
an end-unto-itself. Rolston, too, understands this. But contemporary biology, or at least some of its ideologues and journalists, have
proclaimed that we have long since eradicated the challenge of
teleology by accounting for it on a material basis, i.e., that of the
gene. But the materiality of the gene, i.e., molecular biology, reveals
no such thing. Analysis of the molecular gene has not provided
the laws of generation and variation relevant to evolutionary
change—rather it has revealed the limits of looking at DNA alone.
Insights into the developmental basis of evolutionary variation are
beginning to emerge from studies in cell and developmental biology
but are far from complete. To the extent that cell biology and
evolutionary-developmental (‘‘evo-devo’’) biology always presuppose a preexisting purposeful cell, the complete materialization of
final cause will in fact continue to be a desideratum for some time
to come. Rolston has simply followed a well-traveled path with
antecedents going back to the seventeenth century. Where our grasp
of material cause is not adequate to explain the finality of the living
organism, a transcendent formal (and final) cause, now called
information or the cybernetic gene, is hypostatized. It is the genes,
as Rolston tells us, that ‘‘have a telos.’’
Rolston’s justification for elevating genes to the level of immaterial,
cybernetic/informational quasi-agents is that George C. Williams and
John Maynard Smith said it was so. But why would any biologists be
tempted to think that this could be a scientifically tenable view? I have
argued in earlier work1 that this temptation is rooted in a tendency to
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conflate two different senses of the gene, each of which is valid in a
certain disciplinary domain, but with the proviso that nothing or
almost nothing counts as a gene simultaneously in both senses. Gene-P,
I claim, is the sense of a gene when it is defined by a predictive relationship to a phenotype, but a Gene-P is indeterminate with respect to
its material basis (i.e., its DNA sequence) for reasons I will discuss
soon. So any gene that is a ‘‘gene for’’ (such as the BRCA-1 gene for
breast cancer, or the gene for blue eyes, or the gene for Marfan syndrome) would count as a Gene-P. Gene-D by contrast is the sense of a
gene when it is defined by a nucleic acid sequence that provides the
template resource (or information) for some set of potential
downstream polypeptide and/or RNA products. But Gene-D is
indeterminate with respect to phenotypic outcome just because
between variable splicing, co-and post-translational modification,
targeting, and many other contextual factors, the same Gene-D could
be a contributing factor to entirely different, even antithetical, phenotypic outcomes. If this is correct then the only way to construe a
gene as being both a specific and defined molecular sequence and to
have a specific and defined phenotypic outcome is to conflate these
two independent and non-overlapping senses of the gene. The gene
construed by Dawkins (his selfish gene or ‘‘replicator’’) and that of all
those with very similar views (George C. Williams and John Maynard
Smith perhaps?) are just such conflations.
How, one may well ask, can a Gene-P have a predictable phenotypic outcome without having a determinate nucleic acid sequence?
Would it not just be a matter of finding the relevant sequence? To
understand Gene-P, one must step back from what has become
conventional wisdom or expectation. Gene-P phenomena are based
on the absence of an otherwise normal protein or other resource and
what bodies will predictably do, for better or for worse, in the
absence of that normal resource. Gene-P for blue eyes is not information for making blue eyes—it is simply the absence of a necessary
resource for producing brown eye pigment and blue eyes are what
result, they are what developing human bodies do under such circumstances. There are surely many ways of not having the right
sequence resources for making brown eye pigment and any of those
variations would show up as a gene for blue eyes. Another, perhaps
more striking example is that of Marfan Syndrome. Marfan Syndrome was characterized first by the presence of exceptionally long
and tapering fingers and toes. There are many other characteristics
that have come to be associated with it as well (including an enhanced
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susceptibility to aortic aneurisms). Marfan syndrome occurs when a
protein called fibrillin-1 fails to be incorporated into the bodies’
connective tissue. Any genetic lesion which blocks the incorporation
of fibrillin-1 into connective tissue (including mutations in the
fibrillin-1 sequence that prevent its expression) will show up as a gene
for Marfan Syndrome. But no amount of inquiry into the ‘‘information’’ encoded in Gene-P for Marfan syndrome will reveal
anything about how bodies make long tapering fingers and toes.
Genes-P open windows onto the processes of phenotypic plasticity of
the developing organism and, understood properly, could become
invaluable clues into complex and systematic capacities of the phenotype (and the developmental and dynamic etiology of many
diseases). But for those who are perhaps overly eager to find proof
that science has overcome all the challenges of reconciling final cause
with the metaphysical constraints of a post-teleological nature, GeneP merges with Gene-D producing the illusion of a formal cause
written into the genetic code but transcending its materiality. It
is only the conflation of Gene-P with Gene-D that might appear to
‘‘have a telos.’’ What has been abstracted-out and elevated to
an ethereal, formal status by Rolston is the very material capacity
of developing organisms to respond and adapt plastically (albeit
not always successfully) to both internal and external
challenges—capacities that we simply do not fully understand as yet.
Philosophically, what should it mean to address the question
‘‘what is a gene?’’ If Rolston felt that it meant to claim, or vindicate
the claim, that genetics has solved one of the great metaphysical
problems of modern times—even if it meant a departure from
argumentative rigor—Griffiths and Stotz proceed as if that nature of
the task were a done deal, requiring no reflection on questions of
higher level biological meaning or import, but simply a bloodless
exercise in micro-distinction and making definitions. After a sizeable
review, Griffiths and Stotz leave us with the result that molecular
genes are defined in retrospect of a sequence discerned to be used as
the template for some down-stream products—except when they are
not (in which case they are ‘‘nominal’’ genes). If this were all there
was to be said about the meaning of ‘‘gene,’’ would it suggest anything about the larger questions of biology or even about whether
‘‘what is a gene?’’ is the right philosophical question to ask? The
Griffths and Stotz paper is clearly not about such reflections but
rather is about business as usual. The business-as-usual of biologists,
its seems, just is about using the word gene, and the business-as-usual
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of philosophers just is analyzing what biologists mean when they use
the word gene. Surely all disciplinary texts entail a performative
dimension. Not only do they make a claim about some state of affairs
in the world—implicitly and enactively they also make a claim about
what it is to work within a certain discipline and to make claims from
within that discipline. Surely if ‘‘the gene’’ means no more than
Griffiths and Stotz suggest, then we must wonder why we would ever
have asked this question to begin with, or what it means for genes to
mean so little when everyone seems to assume otherwise, or what the
better questions to ask would have been. But Griffiths and Stotz fail
to notice this elephant in the room that they have just decorated. The
performative thrust of their article seems to be something about
philosophers of science getting the (essentially technical) jobs done,
elephants not withstanding.
So is ‘‘what is a gene?’’ the right question to ask? I have suggested
that the cardinal challenge in scientifically understanding life has not
changed since Aristotelian Day One, i.e., accounting for the finality of
living organisms as material beings, and have argued that one cannot
appreciate what the great interest in ‘‘genes’’ has been without
appreciating how genes have been perceived in this larger context. If
‘‘what is a gene?’’ is to be an interesting question, it is only by leading
us to understand how we are currently attending to the big picture and
by pointing in those directions whereby our next inroads are most
likely to be made. Rolston and Griffiths & Stotz have demonstrated
two of the wrong ways of approaching the question and thus of the
liabilities of asking this question itself. Where Rolston has inflated the
concept of the gene with helium and described its ascent into the
heavens, Griffiths & Stotz have deflated it down to where it can be
aliquoted onto a 96 well plate and analyzed spectrophotometrically,
and have insinuated that this is what hard-working philosophers are
meant to do for a living.
Must an analysis of the gene concept necessarily miss the mark of
that big picture that makes ‘‘what is a gene?’’—a question potentially
worth asking to begin with? Inasmuch as the gene concept has been
the leading conceptual device through which 20th century biologists
have attempted to grasp at the inner springs and principles of the
organism, an adequate analysis of its current status should in fact
lead us to understand the state of the science, or perhaps at least to
know where else to look. Griffiths & Stotz claimed to have identified
three senses of the gene, three gene concepts, the first ‘‘instrumental’’
and the other two ‘‘molecular.’’ Had they pursued this line of inquiry,
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they might have been led to more sure-fire results. But in practice
what they did was to squint their eyes and see only their molecular
gene or genes which they could then treat as a narrow and primarily
technical problem in conceptual microanalysis divorced from all of
those big questions about life that had ever made genetics an exciting
enterprise. The idea of ‘‘an instrumental gene’’ bears a superficial
resemblance to a Gene-P, but as a Gene-P it is eviscerated and
confused. What exactly Griffiths and Stotz mean by instrumental
genes playing a ‘‘critical role in the construction and interpretation of
a range of experiments in which the relationship between genotype
and phenotype is explored via hybridization between organisms or
directly between nucleic acid molecules,’’ one can only wonder.
Whatever it is, it is clearly meant to relegate the gene-for-phenotype
sense of the gene concept to some very remote left field where it can
be easily ignored. But the interest in genes has always been associated
with the gene-for effect because this is where there appeared to be a
way to grasp at the complex and apparently purposive capacities of
the organism. Conflating this with molecular genes was the wrong
way to go but once this error has been exposed, Gene-P phenomena
can be set loose as an invaluable point of entry into real biology. We
are starting to develop the conceptual vocabulary for such understanding. It is Gene-P phenomena that can now be most readily
associated with the developmental phenotypic plasticity of living
organisms that are based on the presence of conserved core modular
processes, and the earlier compartmentalization of the embryo, which
can respond to either an external (environmental) or an internal (e.g.,
Gene-P) perturbation, symmetrically, through restructuring modular
interactions. The modular developmental architecture of the organism allows us to understand how mutations can both be buffered and
compartmentally delimited, yet also how they their phenotypic consequences can be amplified, thus making Gene-P effects possible (and
comprehensible). Kirschner and Gerhart (Roe, 1981) refer to this as
‘‘facilitated variation.’’ Mary Jane West-Eberhard, (Shapiro, in press)
whose four-step evo/devo model of phenotype-first evolution contains two distinct roles for genes, one which is Gene-P like, and the
other which is Gene-D like, terms the capacity of an organism to
parlay entirely different phenotypic patterns ‘‘developmental recombination.’’ The concepts of facilitated variation and developmental
recombination first give us the tools for understanding the possibility
of (unconflated) Gene-P phenomenon, the thousands of actual types
of Gene-P phenomena provide cellular, developmental, and
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533
evolutionary-developmental biology with invaluable resources for
fleshing out the actual dynamics of phenotype transitions.
Finally, even at the level of Gene-D, Griffiths & Stotz missed the
(at least more interesting) boat. What is progressively emerging as
perhaps the most surprising and revolutionary characteristic of DNA
is the ability of that major part of the genome described as ‘‘transposable’’ to move, expand, modify, and systematically restructure the
genome and its proclivities. Where most of the fancy bells and
whistles pertaining to splicing and other coding-regulatory phenomena are derived from eukaryotes, the self-triggering mobility and
transformability of DNA was already pervasive in prokaryotes and is
thus coextensive with life as we know it and its apparent finality.
(West-Eberhard, 2003)
If the question ‘‘what is a gene?’’ is bound to bias thinkers and
readers away from dynamic genomes and flexible phenotypes and
toward ‘‘coding regions’’ (or their ‘‘nominal’’ surrogates), then it is
fair to say that ‘‘what is a gene?’’ is indeed the wrong question to ask.
NOTE
1
Online Mendelian Inheritance in Man (OMIM), (http://www.ncbi.nlm.nih.gov/
entrez/query.fcgi?CMD=search&DB=omim), Accessed on September 4, 2006.
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Roe, S.A. Matter, Life, and Generation: 18th century Embryology and the
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Department of Sociology & Philosophy and
ESRC Center for Genomics in Society
University of Exeter Amory BLDG,
Rennes Dr., Exeter
Devon, EX44RJ
UK
E-mail: [email protected]